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MedChemExpress p38 mapk inhibitor sb203580 sb
P38 Mapk Inhibitor Sb203580 Sb, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 98/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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MedChemExpress p38 inhibitor sb203580
P38 Inhibitor Sb203580, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 98/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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MedChemExpress p38 mapk inhibitor sb203580
TLCA regulates mitochondrial biogenesis and altered myofiber type composition through the <t>p38</t> MAPK/PGC-1α signaling pathway. A Cell viability of cells treated with different concentrations of TLCA for 24 h (n = 10). B & F The mRNA expression of MYH1A and MYH7B (n = 6). C & G Intracellular enzymatic activities of succinate dehydrogenase (SDH) and lactate dehydrogenase (LDH), ATP content and mitochondrial DNA (mtDNA) content (n = 6). D & H The mRNA expression of HK1, GPI, PGAM1, PGK1, PYGL, PGC-1α, NRF1 and TFAM (n = 6). E The protein expression of PGC-1α, <t>p38</t> <t>MAPK</t> and phosphorylation p38 MAPK (n = 3). I The protein expression of PGC-1α (n = 3). Data were shown as mean ± SD; *Represents significant difference when compared with 0 μM TLCA or CON group, and # represents significant difference when compared with TLCA group. *& # P < 0.05, ⁎⁎ & ## P < 0.01, ⁎⁎⁎ & ### P < 0.001.
P38 Mapk Inhibitor Sb203580, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 98/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Selleck Chemicals p38 mapk inhibitor sb203580
TNF-α-induced changes in Wnt/β-catenin-related transcripts and activation of the <t>p38-MAPK-CREB</t> signaling pathway in osteocytes. (A) Dot plots showing relative mRNA levels of Ctnnb1 (β-catenin), Lef1 , and Axin2 in MLO-Y4 cells treated with or without TNF-α ( n = 3). (B) Representative immunoblotting images showing phosphorylated p38 MAPK (p-p38), total p38, phosphorylated CREB (p-CREB), total CREB, phosphorylated JNK (p-JNK), total JNK, phosphorylated ERK (p-ERK), total ERK, and β-actin in MLO-Y4 cells following TNF-α treatment. Data in (A) are shown as individual values with the mean ± SD and were analyzed by the two-sided Student’s t -test. (C) Representative immunoblot of OPG in TNF-α-stimulated MLO-Y4 cells treated with a p38 inhibitor or a CREB inhibitor. Cells were stimulated with TNF-α in the presence or absence of <t>SB203580</t> (p38 inhibitor) or 666-15 (CREB inhibitor), and total cell lysates were subjected to immunoblotting for OPG. β-actin serves as the loading control. Numeric values shown beneath each band represent the relative expression levels of OPG/β-actin for the corresponding lane. (D) ChIP-PCR demonstrating enrichment of the OPG promoter in anti-CREB immunoprecipitates from MLO-Y4 cells with or without TNF-α stimulation, with densitometric quantification of the ChIP-PCR bands; input DNA served as the internal control, normal IgG as the negative control, and anti-histone H3 as the positive control.
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TNF-α-induced changes in Wnt/β-catenin-related transcripts and activation of the <t>p38-MAPK-CREB</t> signaling pathway in osteocytes. (A) Dot plots showing relative mRNA levels of Ctnnb1 (β-catenin), Lef1 , and Axin2 in MLO-Y4 cells treated with or without TNF-α ( n = 3). (B) Representative immunoblotting images showing phosphorylated p38 MAPK (p-p38), total p38, phosphorylated CREB (p-CREB), total CREB, phosphorylated JNK (p-JNK), total JNK, phosphorylated ERK (p-ERK), total ERK, and β-actin in MLO-Y4 cells following TNF-α treatment. Data in (A) are shown as individual values with the mean ± SD and were analyzed by the two-sided Student’s t -test. (C) Representative immunoblot of OPG in TNF-α-stimulated MLO-Y4 cells treated with a p38 inhibitor or a CREB inhibitor. Cells were stimulated with TNF-α in the presence or absence of <t>SB203580</t> (p38 inhibitor) or 666-15 (CREB inhibitor), and total cell lysates were subjected to immunoblotting for OPG. β-actin serves as the loading control. Numeric values shown beneath each band represent the relative expression levels of OPG/β-actin for the corresponding lane. (D) ChIP-PCR demonstrating enrichment of the OPG promoter in anti-CREB immunoprecipitates from MLO-Y4 cells with or without TNF-α stimulation, with densitometric quantification of the ChIP-PCR bands; input DNA served as the internal control, normal IgG as the negative control, and anti-histone H3 as the positive control.
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Cell Signaling Technology Inc p38 inhibitor sb203580
TNF-α-induced changes in Wnt/β-catenin-related transcripts and activation of the <t>p38-MAPK-CREB</t> signaling pathway in osteocytes. (A) Dot plots showing relative mRNA levels of Ctnnb1 (β-catenin), Lef1 , and Axin2 in MLO-Y4 cells treated with or without TNF-α ( n = 3). (B) Representative immunoblotting images showing phosphorylated p38 MAPK (p-p38), total p38, phosphorylated CREB (p-CREB), total CREB, phosphorylated JNK (p-JNK), total JNK, phosphorylated ERK (p-ERK), total ERK, and β-actin in MLO-Y4 cells following TNF-α treatment. Data in (A) are shown as individual values with the mean ± SD and were analyzed by the two-sided Student’s t -test. (C) Representative immunoblot of OPG in TNF-α-stimulated MLO-Y4 cells treated with a p38 inhibitor or a CREB inhibitor. Cells were stimulated with TNF-α in the presence or absence of <t>SB203580</t> (p38 inhibitor) or 666-15 (CREB inhibitor), and total cell lysates were subjected to immunoblotting for OPG. β-actin serves as the loading control. Numeric values shown beneath each band represent the relative expression levels of OPG/β-actin for the corresponding lane. (D) ChIP-PCR demonstrating enrichment of the OPG promoter in anti-CREB immunoprecipitates from MLO-Y4 cells with or without TNF-α stimulation, with densitometric quantification of the ChIP-PCR bands; input DNA served as the internal control, normal IgG as the negative control, and anti-histone H3 as the positive control.
P38 Inhibitor Sb203580, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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TLCA regulates mitochondrial biogenesis and altered myofiber type composition through the p38 MAPK/PGC-1α signaling pathway. A Cell viability of cells treated with different concentrations of TLCA for 24 h (n = 10). B & F The mRNA expression of MYH1A and MYH7B (n = 6). C & G Intracellular enzymatic activities of succinate dehydrogenase (SDH) and lactate dehydrogenase (LDH), ATP content and mitochondrial DNA (mtDNA) content (n = 6). D & H The mRNA expression of HK1, GPI, PGAM1, PGK1, PYGL, PGC-1α, NRF1 and TFAM (n = 6). E The protein expression of PGC-1α, p38 MAPK and phosphorylation p38 MAPK (n = 3). I The protein expression of PGC-1α (n = 3). Data were shown as mean ± SD; *Represents significant difference when compared with 0 μM TLCA or CON group, and # represents significant difference when compared with TLCA group. *& # P < 0.05, ⁎⁎ & ## P < 0.01, ⁎⁎⁎ & ### P < 0.001.

Journal: Poultry Science

Article Title: Gut microbiota-derived taurolithocholic acid modulates myofiber-type switching via p38 MAPK/PGC-1α signaling underlying breed differences between Arbor Acres and Taoyuan chickens

doi: 10.1016/j.psj.2026.106914

Figure Lengend Snippet: TLCA regulates mitochondrial biogenesis and altered myofiber type composition through the p38 MAPK/PGC-1α signaling pathway. A Cell viability of cells treated with different concentrations of TLCA for 24 h (n = 10). B & F The mRNA expression of MYH1A and MYH7B (n = 6). C & G Intracellular enzymatic activities of succinate dehydrogenase (SDH) and lactate dehydrogenase (LDH), ATP content and mitochondrial DNA (mtDNA) content (n = 6). D & H The mRNA expression of HK1, GPI, PGAM1, PGK1, PYGL, PGC-1α, NRF1 and TFAM (n = 6). E The protein expression of PGC-1α, p38 MAPK and phosphorylation p38 MAPK (n = 3). I The protein expression of PGC-1α (n = 3). Data were shown as mean ± SD; *Represents significant difference when compared with 0 μM TLCA or CON group, and # represents significant difference when compared with TLCA group. *& # P < 0.05, ⁎⁎ & ## P < 0.01, ⁎⁎⁎ & ### P < 0.001.

Article Snippet: The differentiation medium containing TLCA and p38 MAPK inhibitor SB203580 (152121-47-6, MedChemExpress, Shanghai, China) was added to CPMs after 4 days of differentiation, and the cells were collected after 24 h.

Techniques: Expressing, Phospho-proteomics

TNF-α-induced changes in Wnt/β-catenin-related transcripts and activation of the p38-MAPK-CREB signaling pathway in osteocytes. (A) Dot plots showing relative mRNA levels of Ctnnb1 (β-catenin), Lef1 , and Axin2 in MLO-Y4 cells treated with or without TNF-α ( n = 3). (B) Representative immunoblotting images showing phosphorylated p38 MAPK (p-p38), total p38, phosphorylated CREB (p-CREB), total CREB, phosphorylated JNK (p-JNK), total JNK, phosphorylated ERK (p-ERK), total ERK, and β-actin in MLO-Y4 cells following TNF-α treatment. Data in (A) are shown as individual values with the mean ± SD and were analyzed by the two-sided Student’s t -test. (C) Representative immunoblot of OPG in TNF-α-stimulated MLO-Y4 cells treated with a p38 inhibitor or a CREB inhibitor. Cells were stimulated with TNF-α in the presence or absence of SB203580 (p38 inhibitor) or 666-15 (CREB inhibitor), and total cell lysates were subjected to immunoblotting for OPG. β-actin serves as the loading control. Numeric values shown beneath each band represent the relative expression levels of OPG/β-actin for the corresponding lane. (D) ChIP-PCR demonstrating enrichment of the OPG promoter in anti-CREB immunoprecipitates from MLO-Y4 cells with or without TNF-α stimulation, with densitometric quantification of the ChIP-PCR bands; input DNA served as the internal control, normal IgG as the negative control, and anti-histone H3 as the positive control.

Journal: JBMR Plus

Article Title: Osteocytes regulate osteoprotegerin expression via the p38-MAPK-CREB pathway in rheumatoid arthritis

doi: 10.1093/jbmrpl/ziag023

Figure Lengend Snippet: TNF-α-induced changes in Wnt/β-catenin-related transcripts and activation of the p38-MAPK-CREB signaling pathway in osteocytes. (A) Dot plots showing relative mRNA levels of Ctnnb1 (β-catenin), Lef1 , and Axin2 in MLO-Y4 cells treated with or without TNF-α ( n = 3). (B) Representative immunoblotting images showing phosphorylated p38 MAPK (p-p38), total p38, phosphorylated CREB (p-CREB), total CREB, phosphorylated JNK (p-JNK), total JNK, phosphorylated ERK (p-ERK), total ERK, and β-actin in MLO-Y4 cells following TNF-α treatment. Data in (A) are shown as individual values with the mean ± SD and were analyzed by the two-sided Student’s t -test. (C) Representative immunoblot of OPG in TNF-α-stimulated MLO-Y4 cells treated with a p38 inhibitor or a CREB inhibitor. Cells were stimulated with TNF-α in the presence or absence of SB203580 (p38 inhibitor) or 666-15 (CREB inhibitor), and total cell lysates were subjected to immunoblotting for OPG. β-actin serves as the loading control. Numeric values shown beneath each band represent the relative expression levels of OPG/β-actin for the corresponding lane. (D) ChIP-PCR demonstrating enrichment of the OPG promoter in anti-CREB immunoprecipitates from MLO-Y4 cells with or without TNF-α stimulation, with densitometric quantification of the ChIP-PCR bands; input DNA served as the internal control, normal IgG as the negative control, and anti-histone H3 as the positive control.

Article Snippet: For inhibitor experiments, the p38 MAPK inhibitor SB203580 (Selleck Chemicals) was used at a concentration of 30 μM, and the CREB inhibitor 666-15 (Selleck Chemicals) was used at a concentration of 0.1 μM.

Techniques: Activation Assay, Western Blot, Control, Expressing, Negative Control, Positive Control